Tehran University Medical Journal

Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: Ample evidence indicated that glucocorticoids, when administered after training, enhance memory consolidation in a variety of tasks. The mechanisms underlying the enhancing effects of glucocorticoids on memory consolidation are not well known. The aim of this study was to determine the role of NMDA receptors and calcium channels in glucocorticoid-induced enhancement of avoidance memory consolidation in mice.
Methods: Experiments were performed on 166 male albino mice (about 30gr). The animals were trained in an inhibitory avoidance (IA) task (0.5mA shock for 3 seconds). In Experiment 1, dose- response effects of corticosterone on memory consolidation were determined. Immediately after training in IA task, the animals were received different doses of corticosterone (0.3, 1 or 3mg/kg). In Experiments 2 and 3, effects of corticosterone on memory consolidation were examined in the presence or absence of verapamil, a calcium channel blocker, (2.5, 5 or 20mg/kg) or MK-801, an antagonist of NMDA receptor (0.1mg/kg), respectively. In all experiments, retention test was done two days later.
Results: Results from first experiment revealed that corticosterone at dose of 0.3mg/kg significantly improved consolidation of avoidance. Data from experiments 2 and 3 showed that both verapamil, in doses of 2.5 and 5mg/kg, and MK801 significantly blocked corticosterone-induced enhancement of memory consolidation.
Conclusion: Finding of this study clearly demonstrated that the memory enhancing effects of corticosterone, at least in part mediate via calcium channels and NMDA receptors.